Hepatitis D virus—can only infect cells previously infected with hepatitis B. 
 Delta hepatitis (HDV) is associated with a 35-nm RNA virus composed of a delta antigen-bearing core surrounded by HBV's Ag coat;

HDV requires HBV for replication.

Delta hepatitis can cause quiescent HBV states to suddenly worsened . Its transmission is the same as that of HBV.
 
 Hepatitis E virus—a high mortality rate in infected pregnant women.

Hepatitis E (HEV) is caused by a single-stranded RNA virus. The disease is typically self-limited and does not evolve into chronic hepatitis; it may, however, be cholestatic.

Pregnant women may develop fulminant disease.

Transmission is by the fecal oral route.

HEV occurs mainly in India, Nepal, Pakistan, and Southeast Asia.
 

Cholecystitis 
 
It is inflammation of the gall bladder. It may be acute or chronic.
In 80-90% of cases, it is associated with gall stones (Calcular cholecystis). 

Causes and pathogenesis:-
Obstruction of cystic or common bile duct- By stones, strictures, pressure from the outside, tumors etc.
Obstruction , chemical irritation of the gall bladder, Secondary bacterial infection, stone formation, trauma to the wall of gall
bladder 

Secondary bacterial infection

Usually by intestinal commensals E.coli, streptococcus fecalis. They reach the gall bladder by lymphatics. 
S.typhi reaches the gall bladder after systemic infection

Acute cholecystitis

Gall bladder is enlarged edematous and fiery red in color. 
- Wall is edematous, hyperemic, may show abscesses or gangrenous dark brown or green or black foci which may perforate.
Serous covering show fibrinosuppurative inflammation and exudation. Mucosa is edematous, hyperemic and ulcerated.
- If associated with stones, obstruction results in accumulation of pus leading to Empyaema of the gall bladder.

Fate:-  Healing by fibrosis and adhesions.

Complications:-  
- Pericholecystic abscess.
- Rupture leading to acute peritonitis.
- Ascending suppurative cholangitis and liver abscess 

Chronic cholecystitis
May follow Acute cholecystitis or starts chronic. Gall stones are usually present. 

Pathology

1. If associated with obstruction: Gall bladder is dilated. Wall may be thickened or thinned out. Contents may be clear, turbid or purulent. 
2. If not associated with obstruction: - Gall bladder is contracted, wall is markedly thickened.
3. Serosa is smooth with fibrous adhesions. Draining lymph nodes are enlarged.  
4. Wall is thickened, opaque and gray-white with red tinge.
5. Mucosa is gray- red with ulcerations and pouches.
6. Stones are usually present

Clinical & biologic death

Clinical death

Clinical death is the reversible transmission between life and biologic death. Clinical death is defined as the period of respiratory, circulatory and brain arrest during which initiation of resuscitation can lead to recovery.

Signs indicating clinical death are

• The patient is without pulse or blood pressure and is completely unresponsive to the most painful stimulus.

• The pupils are widely dilated

• Some reflex reactions to external stimulation are preserved. For example, during intubations, respiration may be restored in response to stimulation of the receptors of the superior laryngeal nerve, the nucleus of which is located in the medulla oblongata near the respiratory center.

• Recovery can occur with resuscitation. 

Biological Death

Biological death (sure sign of death), which sets in after clinical death, is an irreversible state

of cellular destruction. It manifests with irreversible cessation of circulatory and respiratory

functions, or irreversible cessation of all functions of the entire brain, including brain stem.

THE ADRENAL GLANDS 
ADRENAL CORTEX 
The adrenal cortex synthesizes three different types of steroids: 
1. Glucocorticoids (principally cortisol), which are synthesized primarily in the zona fasciculata 
2. Mineralocorticoids, the most important being aldosterone, which is generated in the zona glomerulosa; and 
3. Sex steroids (estrogens and androgens), which are produced largely in the zona reticularis.  

ADRENAL MEDULLA

The adrenal medulla is populated by cells derived from the neural crest (chromaffin cells) and their supporting (sustentacular) cells. 
They secrete catecholamines in response to signals from preganglionic nerve fibers inthe sympathetic nervous system.

Herpes simplex is subdivided into type 1 and 2, the former usually developing lesions around the lips and mouth and the latter producing vesicular lesions in the genital region 
 - contracted by physical contact; incubation 2-10 days.
 - primary HSV I usually is accompanied by systemic signs of fever and Lymphadenopathy, while recurrent herpes is not associate with systemic signs.
 - dentists often become infected by contact with patient saliva and often develop extremely painful infections on the fingers (herpetic whitlow).
 - Herpes viruses remain dormant in sensory ganglia and are reactivated by stress, sunlight, menses, etc. 

 - Herpes gingivostomatitis is MC primary HSV 1 infectionÆpainful, vesicular eruptions that may extend for the tongue to the retropharynx.
 - Herpes keratoconjunctivitis (HSV 1)
 - Kaposi's varicelliform eruption refers to an HSV 1 infection superimposed on a previous dermatitis, usually in an immunodeficient person.
 - laboratory: culture; ELISA test on vesicle fluid; intranuclear inclusions within multinucleated squamous cells in scrapings (Tzanck preps) of vesicular lesions. 

Diseases from Str. pyogenes (Group A strep)

1.  Streptococcal pharyngitis.  Most frequent Group A infection.  Throat has gray-white exudate.  Infection may become systemic into blood, sinuses, jugular vein, meninges.  In less than a week the M-protein and capsule production decrease, and transmission declines.

2.  Skin infections, such as impetigo.  Especially in children.  Different M-proteins than in pharyngitis.  Skin infections associated with edema and red streaking (characteristic).

3.  Necrotizing fasciitis/myositis.  Infection of deeper tissue advances despite antibiotics.

4. Scarlet fever.  Caused by phage-associated erythrogenic toxin-producing strains.  Toxins cause cardiac, renal, and other systemic failures.  Rash is very red with a sand-papery feel and shedding of superficial skin.

5.  Toxic Shock Syndrome.  Parallels the toxic shock caused by TSST-carrying Staph. aureus.

6.  Non-suppurative, post-infection diseases. 

Rheumatic fever (myocarditis, cardiac valve disease, polyarthralgia, rashes.  Occurs two  weeks after a pharyngeal infection)

Glomerulonephritis (Occurs two weeks after pharyngeal or skin infections.  Often due to immunologic reaction to M-protein type 12)